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Wound tissue encompasses the dynamic microenvironment of injured skin or soft tissue, characterized by a sequence of overlapping phases: hemostasis, inflammation, proliferation, and remodeling. It involves coordinated actions of platelets, neutrophils, macrophages, fibroblasts, keratinocytes, and endothelial cells, regulated by growth factors like PDGF, TGF-α/β, EGF, and VEGF, which drive chemotaxis, mitogenesis, angiogenesis, and extracellular matrix (ECM) synthesis. In healthy repair, provisional fibrin clots are replaced by granulation tissue rich in collagen and fibronectin, culminating in scar formation, but dysregulation leads to chronic wounds seen in diabetes, vascular disease, or pressure injuries. These chronic states feature persistent inflammation, stalled re-epithelialization, bacterial biofilms, and molecular signatures like upregulated PITX1 or impaired vessel formation. While not a discrete druggable target, wound tissue responses are therapeutically influenced through topical growth factors (e.g., PDGF for diabetic ulcers) or anti-inflammatory agents, though challenges include off-target fibrosis from TGF-β overstimulation and variable healing due to patient comorbidities. Emerging insights from RNA-seq highlight subregion-specific profiles (bed, border, peri-wound), aiding precision interventions.
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